Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system that is thought to be an autoimmune consequence of a microbial infection in a genetically susceptible host. MS patients tend to be immune hyper-responders to a variety of microbial and self antigens, suggesting an element of immune dysregulation in this disease. Little is known about the mechanisms through which this pathologic inflammatory response is generated and maintained. Differential display was performed to screen peripheral blood mononuclear cells (PBMCs) from identical twins that are discordant for MS. An initial screen of a gene amplified only from the MS twin demonstrated an expression rate of 78 percent of MS patients, but only 33 percent of healthy controls. The more precise examination of this gene?s expression using real-time RT-PCR will be followed by a characterization of the gene, including its tissue and organ distribution, the completion of its sequencing, and the identification of the introns and exons in the genomic DNA. Following these studies, the 5? regulatory region of the gene will be characterized and an in vitro transcription and translation product will be generated. Treatments aimed at correcting the over-expression of this gene in MS patients may serve to lessen disease severity or even halt disease progression.